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Category specificity in normal episodic learning: applications to object recognition and category-specific agnosia.

Studies of patients with category-specific agnosia (CSA) have given rise to multiple theories of object recognition, most of which assume the existence of a stable, abstract semantic memory system. We applied an episodic view of memory to questions raised by CSA in a series of studies examining normal observers' recall of newly learned attributes of familiar objects. Subjects first learned to associate arbitrarily assigned colors or textures to objects in a training phase, and then attempted to report the newly learned attribute of each object in a recall task. Our subjects' pattern of recall errors was similar both quantitatively and qualitatively to the identification deficits among patients with CSA for biological objects. Furthermore, errors tended to reflect conceptually and structurally based confusions. We suggest that object identification involves recruitment and integration of information across distributed episodic memories and that this process is susceptible to interference from objects that are structurally similar and conceptually related.

Agnosia↗

Grasping what is graspable: evidence from visual form agnosia.

Patient DF has profound visual form agnosia. Despite this, she has no problem adjusting her finger-thumb grip aperture to the width of objects when reaching to grasp them. In a previous study, however, she was found to have great difficulty in scaling her grip aperture when attempting to grasp a transparent disc through two holes cut into it. This problem was attributed to a putative difference between the visual processing of size and distance in the brain, whereby DF retained the capacity for processing object size but not the separation between distinct elements such as holes. In the present study we have tested this idea more directly, and found no evidence to support such a distinction. Nonetheless, we replicated our earlier finding that DF is unable to produce normal prehension movements when attempting to grasp transparent stimuli by placing her digits into holes. We suggest that, whilst some simple objects offer themselves directly to the dorsal stream for grasping, an intact ventral stream is required to respond appropriately to more complex stimuli.

Adult↗

Associative visual agnosia resulting from a disconnection between intact visual memory and semantic systems.

We report the case of a patient (RC) who developed a severe visual agnosia, associated to alexia without agraphia, color anomia and amnesia, following an ischemic stroke in the territory supplied by the left posterior cerebral artery. Based on his proficient performance on tests evaluating analysis of elementary visual features, formation of viewer-centered and object-centered representations of visual stimuli and discrimination between drawings representing real and unreal objects, we concluded that the critical locus of deficit was a disconnection between the normally functioning visual memory store and the semantic system. RC's disturbance in visual processing of human faces paralleled his recognition disorder of other classes of objects. The possible contribution of neurobiological factors in determining RC's agnosic deficit is discussed.

Aged↗

Optic aphasia with pure alexia: a mild form of visual associative agnosia? A case study.

A single-case study is reported of a naming disorder selective to the visual modality. The patient showed intact access to structural knowledge of objects and letters, but impaired access to complete semantic knowledge of objects and alphabetical knowledge of letters from visual input. The impairment was most striking when the patient had to discriminate between semantically similar objects or within a given symbolic repertoire, i.e. letters. The co-occurrence of a partial deficit of visual recognition for objects and for letters indicated features of optic aphasia and pure alexia. This symmetric performance between object and letter processing may also constitute a mild form of visual associative agnosia.

Aged↗

Visual associative agnosia and optic aphasia. A single case study and a review of the syndromes.

The case is presented of a patient who showed visual naming disturbances caused by a left occipital infarction. His performance on tests of visual naming, of recognition not requiring a verbal response, and of verbal-visual matching demonstrated a wide range of qualitatively different errors, including complete inability to recognize the object, access to partial semantic knowledge, and mere name finding difficulty. On the basis of the present case and of a review of the recent literature, the clinical distinction between visual associative agnosia and optic aphasia and the relation of these disorders with the anatomical site of lesion are discussed.

Agnosia↗

Visual agnosia in an artist.

This report describes a 73 year old left-handed male artist who presented with agnosic symptoms following an occipital cerebral vascular accident. Against a background of a memory disturbance, but otherwise essentially intact linguistic and cognitive capacities, the patient was generally unable to identify single objects on visual presentation, and displayed marked difficulty in interpreting complex objects, depicted scenes, and partially occluded figures. The patient's preserved ability to recognize geometric forms, to perceive optical illusions, and to copy designs, and objects with considerable accuracy suggested the clinical picture of visual agnosia. An examination was undertaken of the effects of this recognition disorder on the artist's capacity to draw. Despite an inability to recognize an object or scene, the patient retained various techniques (perspective, shadowing, designation of texture) which allowed him to copy the display in a veridical fashion. When displays were recognized, or when the patient was given only the name of the object and asked to draw it, he adopted a less slavish approach, characteristic of his pre-morbid artwork. While his post-morbid drawings bore a strong similarity to his earlier works, such features as insufficient differentiation of figure from ground, over-elaboration of detail, and areas of neglect revealed the debilitating effects of the recognition disorder. Moreover, an examination of the patient's strategies revealed numerous compensatory verbal and motor procedures which guided his drawing. Acknowledgments. We wish to acknowledge Dr. Prather Palmer, J.R.'s neurologist, for his cooperation and for making available his very thorough examination notes. Thanks also to Dr. Kent Stevens for providing the stereograms, and to Dr. Frank Benson and Dr. Edgar Zurif for their helpful comments on the manuscript.

Aged↗

Unilateral visual agnosia.

A case of unilateral visual agnosia for all types of stimuli limited to the left visual hemifield and associated with a right occipital temporal vascular lesion is reported. Questions raised by this case of hemiagnosia as compared to previous ones are discussed.

Agnosia↗

A disorder of lightness discrimination in a case of visual form agnosia.

Benson and Greenberg (1969) described an "agnosic" patient whose severe visual recognition disorder could be accounted for in terms of a deficit in the perception of shape. We report here on a recent case of this disorder (visual form agnosia), and have found that she performs very poorly on tasks of discriminating shades of grey, although she is able to discriminate between hues. This sensory deficit helps to explain some of her perceptual difficulties; it also provides further evidence for parallel feature-processing in the human brain complementary to and consistent with recent physiological data on the visual cortex in animals.

Adult↗

Auditory perception in auditory neuropathy: clinical similarity with auditory verbal agnosia.

The precise features of auditory perception in patients with auditory neuropathy have not been well described. In the present study, we examined auditory perception in a patient with auditory neuropathy. The patient was a right-handed 7-year-old boy. His chief complaint was delayed speech and suspected of verbal learning disability. He could talk, read and repeat rather fluently but could not understand fully what was asked. V-IQ, P-IQ and F-IQ of Wechsler Scale for Children III-R were 53, 118 and 81, respectively. Pure tone audiogram was completely normal. His speech discrimination ability was very poor. He could identify environmental sounds with visual matching. He could differentiate intensity difference but not time difference. This phenomenon was reported in patients with hemispheric symptoms. These clinical features are very similar to verbal auditory agnosia. ABR showed no response at 90dBnHL alternating clicks and tone bursts. Click evoked and distortion product otoacoustic emissions (OAE) were normal. Electrocochleogram was also normal. Motor and sensory nerve conduction velocity was completely normal. Pa of MLR and N1 of SVR were present. His diagnosis should be "pure type" of auditory neuropathy or auditory nerve disease. Importance of both ABR and OAE examination should be widely announced and auditory neuropathy must be campaigned stressed to be clinical entity among personnel who take care of children with speech delay.

Agnosia↗

Computerized axial tomography in clumsy children with developmental apraxia and agnosia.

Fifty-one children who were clumsy because of perceptual disabilities and/or defects of motor organization were surveyed with computerized axial tomographic (CT) head scanning and compared to 33 controls by using both linear measurements and visual appraisal of the scans. Thirty-nine percent of these so-called clumsy children described as having developmental apraxia and agnosia, compared to 9% of the controls, were either abnormal or normal variants. These presumed abnormalities included ventricular dilatation, peripheral atrophy and parenchymal lesions. The Evans Ratio and Intercaudate Distance in the clumsy children were not significantly different from the controls, but the Ventricular Area Index was found to be very significantly different in the two groups.

Agnosia↗

Parallel pattern processing and visual agnosia.

A series of visual search experiments are reported examining pattern processing in a visual agnosic patient. We examined search for targets defined by: (I) the combination of their features relative to homogeneous distractors; (2) the combination of their features relative to heterogeneous distractors; and (3) a single feature difference relative to the distractors (their orientation). Normal subjects demonstrate evidence of spatially parallel search when combined-feature targets are detected against homogeneous distractors, and when targets are defined by a salient feature difference. There are non-linear effects of the number of distractors present, and absent responses can be as fast as present. In contrast, search times for combined-feature targets amongst heterogeneous distractors increase linearly with display size, with the slope for absent responses about twice that for present. The contrast between search for combined-feature targets amongst homogeneous and heterogeneous distractors can be attributed to the effects of grouping between distractors and between distractors and targets (Duncan & Humphreys, 1989, 1992; Humphreys & Muller, in press). Grouping between homogeneous distractors facilitates search. An agnosic patient, HJA, showed normal search functions for single-feature targets and for combined-feature targets amongst heterogeneous distractors. However, he was impaired at search for combined-feature targets amongst homogeneous distractors. This suggests that HJA is selectively impaired at grouping conjunctions of form features. The relations between HJA's agnosia and his problem in the parallel grouping of form conjunctions are discussed, as are the implications of the work for understanding normal vision.

Adult↗

Acquired auditory verbal agnosia and seizures in childhood.

The syndome of acquired aphasia with associated seizures in children has been known since the first report in 1957. Since then, 42 cases have been reported. This paper presents a review of these cases and discusses clinical features of three additional children in whom the specific syndrome of auditory verbal agnosia was identified. Presenting features, medical and neurological findings, and results of detailed psychometric and speech and language evaluations are discussed. The syndrome should be suspected in any child who develops loss of previously acquired language, preceded, accompanied, or followed by seizures. Joint diagnostic evaluation and therapeutic planning by neurologists, speech-language pathologists, and teachers are recommended.

Adolescent↗

[Hemianopsia and agnosia].

Hemianopsia and agnosia, the coexistence of a disorder of perception and a disorder of recognition, is exemplified by two patients chosen for their clinical similarity. These two patients each had a stroke, one of the left and the other of the right posterior cerebral artery, resulting right and left hemianopsia respectively. Primary visual functions such as visual acuity and contrast sensitivity were intact. The differences were only apparent as regards the severity of the agnostic disorders. The patient with the lesion on the left failed to recognize stylized drawings, was alexic, could not lipread and was color anomic, but could easily identify handwriting, faces, and voices. The patient with the right posterior lesion could not recognize handwriting, was prosopagnosic and topographagnosic, but had no difficulty in reading, lipreading, or in recognizing stylized drawings. The apparent double dissociation of function demonstrates the presence of two different visual processing mechanisms which are very probably peculiar to the visual system of the left hemisphere in the one case and to that of the right hemisphere in the other. The authors' findings suggest that the two cerebral hemispheres differ fundamentally in the way they process visual information.

Agnosia↗

Neuropathology of auditory agnosia following bilateral temporal lobe lesions: a case study.

Our patient was first diagnosed with auditory agnosia following his second cerebral vascular accident (CVA) in 1975 when he was 37 years old. Comprehensive follow-up examinations of auditory function were periodically conducted until his sudden death 15 years later. His brain was studied postmortem for neuropathology. Initial pure-tone audiometry revealed moderate sensorineural hearing loss in the right ear and mild sensorineural hearing loss in the left ear. However, repeated pure-tone audiometry revealed that thresholds became progressively poorer over time, bilaterally. Speech audiometry of both ears consistently revealed that the patient was unable to discriminate any monosyllabic words (i.e. speech intelligibility scores were 0%, bilaterally). In general, speech and hearing tests demonstrated that he could not comprehend spoken words, but could comprehend written commands and gestures. Postmortem neuropathological study of the left hemisphere revealed total defect and neuronal loss of the superior temporal gyrus, including Heschl's gyrus, and total gliosis of the medial geniculate body. In the right hemisphere, examination revealed subcortical necrosis, gliosis in the centre of the superior temporal gyrus and partial gliosis of the medial geniculate body. The pathological examination supports clinical results in which the patient's imperception of speech sounds, music and environmental sounds could be caused by progressive degeneration of bilateral medial geniculate bodies.

Adult↗

Magnetoencephalography and positron emission tomography studies of a patient with auditory agnosia caused by bilateral lesions confined to the auditory radiations.

The aim of this study was to investigate auditory cortex function in the context of auditory stimuli in a patient with auditory agnosia due to bilateral lesions confined to the auditory radiations. A male patient experienced mild left temporal hemiplegia because of right putaminal hemorrhage at the age of 43 years. Thereafter he recovered completely but hypertension persisted. When he was 53 years old, he suffered left putaminal hemorrhage and went into a coma. After recovering from the coma and right hemiplegia he could hear but could not discriminate speech sounds. Brain CT and MRI demonstrated small bilateral lesions confined to the auditory radiations. Magnetoencephalography demonstrated the disappearance of middle latency responses and auditory-evoked potential studies showed a very small Pa peak. In contrast, a positron emission tomography study demonstrated a marked increase in blood flow in the bilateral auditory cortex in response to both click and monosyllable stimuli. It is speculated that the auditory cortex receives functional projections from the cochlea via non-specific pathways in the cerebral hemispheres.

Agnosia↗

'On mind-blindness (optic agnosia)', a classical clinico-pathological report, and its author Wilhelm von Stauffenberg (1879-1918).

Two photographs from the beginning of our century still instructively illustrate the phenomenon of visual agnosia: the perplexed face of an old lady confronted with objects clears after touching them. This patient with bilateral posterior cerebral infarction was followed for seven years at the Munich Medicine Department of Friedrich von Müller (1858-1941) who had a strong interest in neurology. His assistant Wilhelm von Stauffenberg (1879-1918) reported the case in great detail, including anatomical analysis performed under Constantin von Monakow (1853-1930). Promoted to "Privatdozent" in 1913 on the basis of this report, Stauffenberg's work included several additional, similarly extensive clinico-anatomical case studies but was not limited to problems of cerebral localisation. Under the influence of the Burghölzli group in Zürich he started to practice psychotherapy. Stauffenberg, deeply interested also in the arts and in literature, was the physician of the poet Rainer Maria Rilke (1875-1926) from 1914. He succumbed to pneumonia in 1918.

Agnosia↗

Prosopagnosia and agnosia for noncanonical views. An autopsied case.

It has been postulated that for prosopagnosia to occur, bilateral lesions of the central visual system are usually necessary. All but 1 of the 10 previously documented cases that came to autopsy showed this pattern. However, the long survival period after the onset of prosopagnosia in most of these patients limits the value of the autopsy findings for clinicopathological correlation. A patient is presented who died 10 days after she had developed prosopagnosia, topographagnosia and an agnosia for real objects seen from noncanonical views. These clinical symptoms corresponded directly to the autopsy finding of a recent large occipitotemporal ischaemic infarct in the territory of the right posterior cerebral artery. An additional right frontal infarct and a cortical microinfarct in a deep left lateral parieto-occipital sulcus were both old lesions and had passed unnoticed clinically. This first report of a direct clinicopathological correlation between a fresh right posterior lesion and prosopagnosia demonstrates that bilateral involvement of the visual system is not a prerequisite for prosopagnosia.

Aged↗

Perception and action in 'visual form agnosia'.

A single case study of a patient with 'visual form agnosia' is presented. A severe visual recognition deficit was accompanied by impairments in discriminating shape, reflectance, and orientation, although visual acuity and colour vision, along with tactile recognition and intelligence, were largely preserved. Neuropsychological and behavioural investigations have indicated that the patient is able to utilize visual pattern information surprisingly well for the control of hand movements during reaching, and can even read many whole words, despite being unable to make simple discriminative judgements of shape or orientation. She seems to have no awareness of shape primitives through Gestalt grouping by similarity, continuity or symmetry. It is proposed that many of these perceptual disorders might be the combined result of (1) a selective loss of the cortical elaboration of the magnocellular visual processing stream, and (2) a selective output disconnection from a central processor of visual boundaries and shape primitives in the occipital cortex.

Adult↗